| Original language | English |
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| Article number | ddy434 |
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| Pages (from-to) | 1322-1330 |
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| Number of pages | 9 |
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| Journal | Human Molecular Genetics |
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| Volume | 28 |
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| Issue number | 8 |
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| Early online date | 18 Dec 2018 |
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| DOIs | |
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| Date | Accepted/In press - 30 Nov 2018 |
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| Date | E-pub ahead of print - 18 Dec 2018 |
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| Date | Published (current) - 15 Apr 2019 |
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Given clear evidence that smoking lowers weight, it is possible that individuals with higher body mass index (BMI) smoke in order to lose or maintain their weight.
We performed Mendelian randomization (MR) analyses of the effects of BMI on smoking behaviour in UK Biobank and the Tobacco and Genetics consortium GWAS, on cotinine levels and nicotine metabolite ratio in published GWAS, and on DNA methylation in the Avon Longitudinal Study of Parents and Children.
Our results indicate that higher BMI causally influences lifetime smoking, smoking initiation , smoking heaviness and also DNA methylation at the aryl-hydrocarbon receptor repressor (AHRR) locus, but not smoking cessation. While there is no strong evidence that BMI causally influences cotinine levels, suggestive evidence for a negative causal influence on nicotine metabolite ratio may explain this.
There is a causal effect of BMI on smoking, but the relationship is likely to be complex due to opposing effects on behaviour and metabolism.
- Nicotine, Smoking, body mass index procedure, metabolism, Genome-Wide Association Study, Mendelian randomisation analysis
- Brain and Behaviour
- Tobacco and Alcohol
http://orcid.org/0000-0003-0574-5071